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Dementia Studies by Dr. P. Kongshavn

Neurodegenerative Diseases – Alzheimer’s and Parkinson’s
By Patricia A.L. Kongshavn, Ph.D.
Alzheimer’s and Parkinson’s are neurodegenerative diseases in which cell damage and degeneration is
seen in certain specific areas of the brain. In Parkinson’s disease nerve cells slowly degenerate in the part
of the mid-brain (the substantia nigra layer of the basal ganglia) that controls movement, resulting in
progressive loss of muscular coordination and balance. In Alzheimer’s disease brain cells degenerate,
brain mass shrinks and characteristic neurofibrillary tangles and neural plaques are seen post mortem.
Increasing lines of evidence suggest that mitochondrial damage plays a key role in
Parkinson’s, Alzheimer’s and some other neurodegenerative diseases (1-5). This, in
turn, increases the generation of reactive oxygen species and the onset of oxidative
stress, leading to oxidative damage and programmed cell death.
At the same time, glutathione homeostasis is disturbed (6-9). In one study, glutathione levels were
reduced by 40% in the substantia nigra in early stage Parkinson’s disease (7). These levels fall even
much further in later stages, the magnitude of reduction in glutathione seeming to parallel the severity of
the disease (9). The lowered glutathione values and increased oxidative stress are thought to be
responsible for the loss of dopamine producing cells in the substantia nigra in Parkinson’s disease
patients (7, 8).
The use of antioxidants, particularly glutathione, for the treatment of neurodegenerative diseases is an
obvious consideration (6-9). In an in vitro study, glutathione was shown to protect human neural cells from
apoptosis i.e. cell death, induced by dopamine (8). Sechi et al. showed that intravenous injection of
glutathione was effective in reducing symptoms (42% decline in disability) in early Parkinson’s disease
patients and possibly retarded the progression of the disease (9). Other treatment options to increase
brain concentrations of glutathione are better choices for long-term treatment. Banaclocha has reviewed
the putative usefulness of N-acetyl cysteine for this purpose in the treatment of Parkinson’s, Alzheimer’s
and other age-associated neurodegenerative diseases (1). Immunocal is an even better choice than this
drug, being entirely non-toxic and proven to raise intracellular glutathione (10).
1. Banaclocha, MM. Therapeutic potential of N-acetylcysteine in age-related mitochondrial
neurodegenerative diseases. Med Hypotheses 56:472-477, 2001.
2. Schultz JB, Lindenau J, Seyfried J et al. Glutathione, oxidative stress and neurodegeneration. Eur J
Biochem 267:4904-4911, 2000.
3. Jenner P, Olanow CW Neurology 47:S1161-S170, 1996.
4. Kidd PM. Parkinson’s disease as a multifactorial oxidative neurodegeneration: implications for
integrative management. Altern Med Rev 5:501, 2000.
5. Lohr JB, Browning JA Free radical involvement in neuropsychiatric illnesses. Psychopharmacol Bull
31:159-165, 1995.
6. Reid M, Jahoor F. Glutathione in disease. Curr Opin Clin Nutr Metab Care 4:65-71, 2001.
7. Sian J, Dexter DT, Lees AJ, et al. Alterations in glutathione levels in Parkinson’s disease and other
neurodegenerative disorders affecting basal ganglia. Ann Neurol 348-355, 1994.
8. Gabby M, Tauber M.Porat S et al. Selective role of glutathione in protecting human neuronal cells from
dopamine-induced apoptosis. Neuropharmacology 35:571-578, 1996.
9. Sechi G, Deledda MG, Bua G et al. Reduced intravenous glutathione in the treatment of early
Parkinson’s disease. Prog Neuropsychopharmacol Biol Psychiatry 20: 1159-1170, 1996.
10. Lands L, Grey VL, and Smountas AA Effect of supplementation with a cysteine donor on muscular

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